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Are Limited Lifespans An Evolutionary Adaptation?

evolutionary adaptation limited lifespans aging theory

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#1 sthira

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Posted 26 July 2015 - 01:31 AM


http://io9.com/are-l...tion-1710634703

George Dvorsky
6/12/15 1:00pm

Are Limited Lifespans An Evolutionary Adaptation?

Since the time of Darwin, evolutionary biologists have wondered why the lifespans of different species vary so significantly. A new model now suggests that the life expectancy of any given species is a function of evolutionary pressures — a conclusion that hints at the potential for powerful anti-aging interventions in humans.
The new paper, which now appears in Physical Review Letters, challenges popular conceptions about the nature of aging and why it manifests at different rates in different organisms, including species that are closely related.

By running variations of their model hundreds of thousands of times, a research team led by Yaneer Bar-Yam from the New England Complex Systems Institute (NECSI), in collaboration with the Harvard Wyss Institute for Biologically Inspired Engineering, observed that evolution favors shorter lifespans in environments where resources are scarce and when pressures to procreate are particularly intense. The simulations appeared to show that lifespans of animals — humans included — are genetically conditioned, and not the result of gradual wear-and-tear. It’s a surprising result, one that gives added credence to the burgeoning paradigm known as “programmed aging.” At the same time, the study shows that current efforts to develop anti-aging interventions may be based on incorrect assumptions.

Why We Age

As it stands, there are two prevailing theories that explain “intrinsic mortality,” i.e. death that occurs when an animal dies of “old age” rather than from external causes, such as predation or starvation.
First, there’s the “mutation accumulation” theory posited by Oxford University biologist and Nobel Laureate Peter Medawar. He argued that certain adaptations, or mutations, can produce detrimental effects late in life that are not strongly selected against in evolution. Collectively, these “detrimental” effects manifest as the symptoms of aging and eventually death.

The second theory, called “antagonistic pleiotropy” — or the “pay later theory” — is the idea that a single gene, or characteristic, is beneficial early in life, but then turns detrimental at a later stage. A good example is cellular senescence, which acts beneficially early life by suppressing cancer, but then turns against us later on by causing frailty and, paradoxically, cancer. Antagonistic pleiotropy was conceived by Michigan State University biologist George Williams back in 1957.

There are some problems with these theories, however.

First, they both place an undue emphasis on math — a product of the neo-Darwinian approach to evolution popularized by the likes of Williams and British statistician and mathematician Sir Ronald A. Fisher. The neo-Darwinian synthesis, with its declaration of the gene as the basic unit of evolution, inspired mathematical analyses of phenomena such as kin selection, altruism, and speciation. At the same time, however, the approach has resulted in a subsequent dearth of empirical evidence.

Second, so-called “selfish genes” should work to favor extreme longevity among animals, yet that’s something we don’t observe. As explained to me by Josh Mitteldorf, co-author of the upcoming book, DNA of Death, and an expert on the genetic underpinnings of aging, a primary disadvantage of aging is that an animal eventually dies and leaves less offspring.

Because of these shortcomings, and owing to a growing body of phenomenological data that has been emerging since the 1990s, there’s a third explanation, a theory known as “programmed aging” that was first proposed by biologist August Weismann back in the 1880s. That aging is a deliberate function of our genetics remains a controversial idea, but it’s an idea that’s steadily acquiring adherents.

Programmed Death

One of these adherents is NECSI president Yaneer Bar-Yam, who in the new paper contends that popular approaches to the aging problem fail to address a very important constraint, namely the ways lifespans are genetically controlled according to the resource limitations of a given environment. Without genetically programmed aging, he argues, animals wouldn’t be able to leave sufficient resources for their offspring. And this holds true for all animals, whether they be rabbits, dolphins, or humans.

Are Limited Lifespans An Evolutionary Adaptation?

Mule deer grazing in Zion Canyon. If these creatures had longer lifespans, would there be enough food to go around? (Credit: Itsmine/cc)
Bar-Yam and his team reached this conclusion by developing a simple model that analyzed how the lifespans of simulated organisms would change and evolve over time under spatially constrained conditions.

Instead of looking at the average conditions of environments over time, this model took local variations into account in environments where organisms evolve. In their simulations, the researchers used cellular automata to observe the evolution of lifespan limits and the onset of intrinsic mortality. Though the simulation took place within a tight spatial system, some variables were adjusted, including the presence of self-renewing resources (which in a real life scenario would be akin to the re-growth of grass for grazing animals, available fish stock for dolphins, and so on).

“We simply designed an understanding of what happens when we don’t make the assumption of the same environment,” Bar-Yam told io9. “The only thing it relies upon is spatial locality, which, along with resource limitation, is generally the case in nature.”

Fascinatingly, group selection — the idea that natural selection acts at the group level — was never a consideration in the model. Yet the simulations consistently showed that a built-in life expectancy emerged among the simulated organisms to preserve the integrity of their species over time. This is surprising because a pro-group result was produced via an individualized selectional process.

“Beyond a certain point of living longer, you over-exploit local resources and leave reduced resources for your offspring that inhabit the same area,” Bar-Yam said. “And because of that, it turns out that it’s better to have a specific lifespan than a lifespan of arbitrary length. So, when it comes to the evolution of lifespans, the longest possible lifespans are not selected for.”

Bar-Yam’s work suggests that aging is a mechanism — if not the mechanism — that works to define and limit the lifespans of animals. And if the biological and medical communities can figure out how our genes control these developmental processes, he says we may be able to develop powerful anti-aging interventions. Simply put, the researchers see aging as a genetic disease that can and should be treated.

Tradeoffs and Scaling for Time

These are clearly remarkable claims, so I contacted gerontologist and anti-aging expert Aubrey de Grey to get his take on the paper.

“My initial take is that it’s in line with what is already well known about kin selection and ‘population viscosity,’” he says. “Basically, if one’s nearest relatives are also one’s physically closest neighbours, it’s to be expected that there will be a non-individual benefit from suicide when resources are limited.”

As for the study’s claim that “Intrinsic mortality is not favored for long-range spatial mixing,” de Grey says one can’t extrapolate to any situation in which there’s lots of long-range spatial mixing, “which is of course the case for animals.” On this point de Grey and Bar-Yam disagree, the latter of whom claims that long-range spatial mixing — when two species or populations exist in the same geographic area and regularly encounter and/or compete for resources with one another — is “limited” in the “typical real-world systems.”
de Grey doesn’t buy the programmed aging hypothesis. He recently published a paper at Current Aging Science on this exact topic, concluding that:

...however much we might wish that aging were programmed and thus that the ill-health of old age could be greatly postponed just by disabling some aspect of our genetic makeup, the unfortunate truth is that no such program exists, and thus that our only option for substantial extension of healthspan is a divide-and-conquer panel of interventions to repair the damage that the body inflicts upon itself throughout life as side-effects of its normal operation. I explicitly avoid arguments that rely on unnecessarily abstruse evolutionary theory, in order to render my line of reasoning accessible to the broadest possible audience.
I also contacted S. Jay Olshansky to get his opinion. He’s a professor in the School of Public Health at the University of Illinois at Chicago and Research Associate at the Center on Aging at the University of Chicago.

Here’s what Olshansky said to me in an email:

I would take issue with their final and most important point. If senescence is programmed, manipulating genes to favor greater longevity is likely to have tradeoffs for other attributes of the life history — which the authors never even mention. Since most tradeoffs are negative or undesirable, it is unlikely that such an intervention would actually work. To the contrary, we’re better off without programmed aging — this way, interventions that modulate the rate of senescence (either indirectly or directly) are not battling against a genetic program. Interventions that do not battle against our own genes are more likely to have a substantive impact.

Finally, the authors made the fundamental error of comparing the longevity of species without scaling time. Since species live life on different time scales, failing to scale for time leads some to believe that because the longevity of flies or worms can be increased several fold, therefore the same can be accomplished for humans. My colleague and I wrote an e-book to explain scaled time; unfortunately, it appears to have not been read by these authors. The title is “A Measured Breath of Life”.

I offered Bar-Yam an opportunity to respond to Olshansky’s criticisms.

“That there has to be a tradeoff is exactly what our theory disproves,” he told io9. “The fact that these lifespans are specifically being selected for shows there aren’t such tradeoffs.”

Bar-Yam says it’s true that there might be tradeoffs for particular adaptations, but the mechanism as a whole is precisely and exclusively one of lifespan control.

“And it has to be that way according to the theory — that’s the whole point,” he says. “The theory is telling us that evolution is selecting for that trait in the same way it selects for height, weight, color, and other things. The fact that evolution is selecting for a particular trait implies that there isn’t a necessary tradeoff with other traits.”
To which he added: “The gut reaction from people engaging in this field who feel there have to be tradeoffs are driven by a 40 year old theory that says the only way you can have longer lifespans is by virtue of the fact that there are these tradeoffs.”

As for Olshansky’s point about failing to scale for time, Bar-Yam points to how crocodiles barely seem to age at all, and how some species of birds live for only several years, while others, like the albatross, live for nearly five decades. There are also rockfishes to consider; check out this chart showing the incredible variations in lifespan among its member species:

Are Limited Lifespans An Evolutionary Adaptation?

“There’s no particular lifespan,” he says. “And there’s no reason to believe that particular lifespans have a scale that’s inherent. Lifespans of organisms vary in related species by huge variations.”

Bar-Yam also brought up nematode worms. Researchers have shown that a single gene deletion can extend the lives of these worms by a five-fold increase. Olshansky says it’s not fair or accurate to compare anti-aging interventions between nematodes and humans because of time-scaling. But Bar-Yam argues that time scales are not an important factor.

“If there was a really well defined lifespan, we would be seeing it in a systematic process that would be related to biological size or something else like that, but we don’t really observe that,” he says. “The idea that short lifespans can be extended, but long lifespans cannot, is an idea without a lot of phenomenological support.”
At the same time, there are some biological data points that appear to strengthen the programmed aging hypothesis.

As Josh Mittledorf told me, cellular senescence is a “classic example” of this process at work — a mechanism of programmed death that’s been around ever since the first eukaryotes emerged billions of years ago. There’s also the octopus to consider, an organism that simply stops eating after it’s done reproducing.

“There are many species where death is clearly programmed and there’s no reason for this animal to die,” says Mittledorf.

Implications to Life Extension

The Bar-Yam study was a mathematical, simulation-based investigation of evolution, not a biological one. Consequently, any inferences made by the researchers beyond that — namely those that pertain to potential life extension interventions in humans — need to be taken with a fistful of salt. Biological studies will be required to show if these researchers are on the right track. That said, anti-aging scientists need to take notice.

Are Limited Lifespans An Evolutionary Adaptation?

1
For example, gerontologists like de Grey are working to repair the damage done by aging. Bar-Yam admits that degradation happens over time, but he says biological systems show a remarkable capacity for self-repair.

“The question is, why do self-repairing organisms age?,” he asks. “So in the context of where self-repair is an effective process, why does it not work well enough to keep us alive for 150 to 200 years?”

He says the answer from the traditional theory is not based upon any understanding of biology that tells us aging is necessary, “but it’s only and solely based upon solutions that are based on mathematical approximations.”

Mittledorf says that rather than trying to repair the processes of aging, scientists should try to trick the body into thinking it’s younger. That way, the body will work to repair itself. Experiments in mice, where the blood of the old is replaced with the blood the young, has been shown to reduce the effects of cognitive decline, among other age-related disorders.

“Experiments like these suggest that aging is controlled by factors in the blood, such as hormones and small RNA and gene promoters,” Mittledorf told io9. “Little molecules that stick onto the DNA and program it epigenetically, and then turn on or turn off that gene. We have hundreds, possibly thousands of them in our blood — and they have tremendous influence on the health and destiny of a cell.”

Are Limited Lifespans An Evolutionary Adaptation?

Bar-Yam says there’s both popular hope and fatalism about the nature of aging and death. He claims that many scientists today have placed themselves in direct opposition to the hope, while favoring the fatalism — and they’re doing so by honoring theories based on incorrect assumptions.

“When we remove those assumptions we find that the opposite conclusion is reached,” he says. “So if we have the opposite conclusion, we suddenly have a very different scientific framework that impacts dramatically on the nature of public understanding. It should shift the dialogue dramatically. And that’s really my hope. By shifting the dialogue, I’m hoping we can shift the priorities of analysis of research in a direction that, because of what the theory says, is likely to be a fruitful direction of inquiry.”

Read the entire study at Physical Review Letters:

Programed Death is Favored by Natural Selection in Spatial Systems.
Werfel J, Ingber DE, Bar-Yam Y.
Phys Rev Lett. 2015 Jun 12;114(23):238103. Epub 2015 Jun 12.
PMID: 26196833

Abstract

Standard evolutionary theories of aging and mortality, implicitly based on mean-field assumptions, hold that programed mortality is untenable, as it opposes direct individual benefit. We show that in spatial models with local reproduction, programed deaths instead robustly result in long-term benefit to a lineage, by reducing local environmental resource depletion via spatiotemporal patterns causing feedback over many generations. Results are robust to model variations, implying that direct selection for shorter life span may be quite widespread in nature.

#2 niner

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Posted 26 July 2015 - 02:32 PM

Physicists and mathematicians keep coming up with simplistic computer simulations that "prove" that aging is evolutionarily selected.   These ideas fall apart when one looks even briefly at the real world of predation and infection.

 

Here is a paper that argues against these claims:

 

The evolutionary theory of ageing is generally portrayed as rejecting the notion that ageing has an adaptive basis, i.e. that an age-related decline in survivorship and viability (including reproductive capacity) is favoured by natural selection. Nevertheless, the idea of ‘programmed’ ageing, with its implicit (or occasionally explicit) reliance on an adaptive role, reappears regularly and is commonly expressed by newcomers to the field. The reasons commonly suggested for ageing to be adaptive are: it avoids over-population; it eliminates post-reproductive individuals who would otherwise compete for resources with their younger kin; it facilitates ongoing evolutionary adaptation by promoting succession of generations; and it fits the purported existence of genes ‘for ageing’. The evolutionary logic that establishes that these arguments are, in most cases, fallacious needs to be more widely understood, especially at a time when the discovery of genetic pathways that affect longevity is proceeding apace. At the same time, it needs to be recognised that evolutionary analysis does not, in fact, preclude the possibility that in special circumstances there may be tightly controlled aspects of ageing. Understanding the ways in which natural selection acts on the determinants of longevity is likely to be important in guiding further discoveries that might contribute to efforts to maximise health and wellbeing at later ages.

 

 

It's worth reading.  Full text is available.


Edited by niner, 26 July 2015 - 02:33 PM.


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#3 treonsverdery

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Posted 19 August 2015 - 07:21 PM

One way to view a mathematically based hypothesis is to to see if the opposite is actually opposite, that is do organisms with versions of the math variables at the model they are notably different have a differing effect.  organisms outside of the mathematics of the supposed effect are a beneficial place to find longevity genetics as well as longevity drugs.  The article suggests a mathematics where the organisms persist at the same area finding food.  Whales travel far thus have nonlocal area food supplies. Thus if you were looking to amplify the longevity of a mouse you could find mice with far travel ranges at areas with plentiful food, then see if breeding those with other mice caused greater longevity.  Then genes that are highly similar at humans (haplotypes) could be verified to cause greater longevity.

 

I read that there are large cetaceans, Whales, that live over 200, based on finding centuries old objects at their bodies.  

Rockfish live more than 200 years ( I think I remember 273, yet am not finding that online)



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#4 to age or not to age

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Posted 20 August 2015 - 03:49 PM

I interviewed Dr Steven Austad for my film To Age Or Not to Age.  He had studied Opossums from an island off the southeast coast of the

US who had lost their predators a couple thousand years ago.  Today, the opossums on this island live nearly twice as long as their mainland counterparts, and have an additional litter. Examining the genetics and bio-markers of these close relatives might shed light 

on the above discussion. 

 

 


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#5 Anthropositor

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Posted 23 August 2015 - 10:31 AM

I tend to be more a practical man than a theorist as I age.  My exposure to Aubrey de Grey led me to believe that his specialty was not gerontology but wishful thinking.  It is so easy to get bogged down in endless theories, mathematical models, and reams of scientifically couched jargon, which seems by its' very complexity and verbiage to have some decipherable sense that is just out of reach of straightforward thought.  It is not that I don't like the exercise of a good puzzle or chess problem, but as perhaps one of the oldest people here, I am fairly aware that time is of the essence.  I can sell myself on the notion that living to the age of 125 is not all that much of a long shot.  I am already 3/5 there.  I can not currently persuade myself that there is a prospect of making it to 200.  Nor does that prospect seem particularly appealing.  Past the age of 100, libido is likely to be on the back burner.  Most of you youngsters shudder at the thought that any one thirty or forty years your senior even has a libido, or lets it function with any regularity.  And I have seen not a scintilla of discussion of age discrimination and the social loss of autonomy that will be your lot if you are unlucky enough to become both aged and meaningfully disabled.  Not very realistic. 

 

It is easy to generate counter-arguments to even isolated examples of lifespan increase.  In 1996 the eldest person died at the age of 122.  Since then no one has gotten close.  One would think that in the almost two additional decades since, that record would have been broken several times, or tied by at least a few.  This does not inspire realistic optimism.  One must stir in a big dollop of hope, faith, or wishful thinking.  Okay, I am not entirely above that.  But I will keep in mind that I have added this magical optimism to the equation, and will work to replace it with something more realistic and logical as soon as I can find it.  The goal is not only to live long, but to stave off the ravages that are the lot of many that do manage to delay the grim reaper.

 

Devising ways to continue to have a fun, interesting, meaningful, and socially gratifying life are all essential evolutionary adaptations to extending lifespans markedly.  


Edited by Anthropositor, 23 August 2015 - 10:35 AM.


#6 corb

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Posted 23 August 2015 - 09:51 PM

 

And I have seen not a scintilla of discussion of age discrimination and the social loss of autonomy that will be your lot if you are unlucky enough to become both aged and meaningfully disabled.  Not very realistic.

Most of the discussion we've had throughout the years has focused on exactly that, and as such most of us concluded that longevity, fitness and health are not separate entities and to achieve one you should have control over the others.
We don't talk about age discrimination because we're trying to usher in an age where age related disabilities are, if not non-existent, at least marginalized. Discrimination won't happen if there's nothing to discriminate against - on theory - people are good at finding things to hate so I wouldn't give any guarantees about that.

 

As for super-centenarians not beating the record, it should not come as a surprise.

We do not treat age as a disease or a disability in itself right now. Instead we treat the symptoms of the disabilities it causes and naturally the effect is barely noticeable.

Super-centenarians are few in numbers. So when and if the record for human longevity is beaten is entirely dependent on luck.

 

What we're trying to do as an organization although we're not nearly as organized as we could or should be, is to change the public opinion and to highlight important research and if we're lucky to get some funding to the researchers that need it for pursuing longevity and health.

It doesn't make much sense for you to critique a field of science that's in it's infancy. It's like looking at the first flyer the Wright brothers build and making assumptions about the results that can be achieved. From their wooden planes to the man walking on the moon a lot of money, labour and devotion went into the aeronautic field, in comparison the field of anti-aging has been underfunded and barely staffed and generally looked down upon for decades. I wouldn't say the situation has changed a lot as of late but at least some effort has been made and that's a good sign and maybe even something to look forward to if you're young enough.


Edited by corb, 23 August 2015 - 10:02 PM.

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#7 HighDesertWizard

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Posted 29 August 2015 - 09:22 PM

Are Limited Lifespans An Evolutionary Adaptation?

 

Evolution has not been Selecting For a Single, Specific Trait in Humans... It's been Selecting for Many different Traits in Humans...

 

That said, it turns out...

  • Evolution has been Establishing a Mechanism in Humans that provides increasing capability for manipulation and control of Physical Health and Longevity through Positive Cognition alone.

Evidence Nodes for that Proposition...

  • Higher Heart Rate Variability (HRV) is positively associated with Longevity in Humans

Here’s just one study context... Take a known, Human, Surrogate Marker for Health, it’s a Computed Statistic... Measure this marker for 24 hours in old, wild-type Humans, 65 years old and up with a mean of 73 years… Wait 10 years… 53% of the 347 study animals are now dead... Do some statistical analysis of that surrogate marker data and plot the two survival curves below… That marker, Heart Rate Variability (HRV), has profound implications for human health and longevity... Here’s a link to this study from 1998... Here's a link to more study graphic figures making the same point...

d8RicwD.png

  • The life work of Epel/Blackburn demonstrates at least two things…
  • The life work of Fredrickson(/Cole) demonstrates at least two things...
    • Fredrickson has also found that Positive Emotions increase HRV (http://tinyurl.com/bxqwyym).
    • In another study, Fredrickson/Cole found that individuals with Eudaimonic Intent (aka, Noble Intent, a type of Positive Cognition (Emotion) that contrasts with Hedonic Intent) have reduced NF-kB expression in their peripheral blood (http://tinyurl.com/pzuupxu).
  • Establishing evidence about HRV and its inverse correlation with NF-kB Transcription Activation has been the lifework of Karolinska Institute Honorary Doctorate Kevin Tracey, participant in 440+ studies per ResearchGate.

    • HRV is simultaneously increased with intracellular NF-kB Transcription Inhibition, especially in the Spleen, both via a Vagal-Cholinergic Anti-Inflammatory Pathway (CAIP) mechanism (http://tinyurl.com/nogth6b).
    • I recommend two additional study summaries to get a handle on the basic physiology/biology research that Tracey has spearheaded. (http://tinyurl.com/k7r7vzx and http://tinyurl.com/njy4kl6)
  • Hundreds of studies demonstrate conclusively that Higher HRV is profoundly correlated with Longevity and Lower HRV is profoundly correlated with Morbidity and Mortality. Here are 26 of them.
     
  • ... telomere length robustly predicts longevity, even after factoring out the effect of age, smoking, exercise, blood cholesterol, BMI, and alcohol consumption.  This adds immensely to our knowledge of telomere length and its predictive power...

So there you have it... Some evidence for the Proposition...

  • Evolution has been Establishing a Mechanism in Humans that provides increasing capability for manipulation and control of Physical Health and Longevity through Positive Cognition alone.

Edited by HighDesertWizard, 29 August 2015 - 09:45 PM.


#8 Anthropositor

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Posted 30 August 2015 - 01:24 AM

 

 

And I have seen not a scintilla of discussion of age discrimination and the social loss of autonomy that will be your lot if you are unlucky enough to become both aged and meaningfully disabled.  Not very realistic.

Most of the discussion we've had throughout the years has focused on exactly that, and as such most of us concluded that longevity, fitness and health are not separate entities and to achieve one you should have control over the others.
We don't talk about age discrimination because we're trying to usher in an age where age related disabilities are, if not non-existent, at least marginalized. Discrimination won't happen if there's nothing to discriminate against - on theory - people are good at finding things to hate so I wouldn't give any guarantees about that.

 

As for super-centenarians not beating the record, it should not come as a surprise.

We do not treat age as a disease or a disability in itself right now. Instead we treat the symptoms of the disabilities it causes and naturally the effect is barely noticeable.

Super-centenarians are few in numbers. So when and if the record for human longevity is beaten is entirely dependent on luck.

 

What we're trying to do as an organization although we're not nearly as organized as we could or should be, is to change the public opinion and to highlight important research and if we're lucky to get some funding to the researchers that need it for pursuing longevity and health.

It doesn't make much sense for you to critique a field of science that's in it's infancy. It's like looking at the first flyer the Wright brothers build and making assumptions about the results that can be achieved. From their wooden planes to the man walking on the moon a lot of money, labour and devotion went into the aeronautic field, in comparison the field of anti-aging has been underfunded and barely staffed and generally looked down upon for decades. I wouldn't say the situation has changed a lot as of late but at least some effort has been made and that's a good sign and maybe even something to look forward to if you're young enough.

 

 



#9 Anthropositor

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Posted 30 August 2015 - 04:31 AM

The above answer left out my comprehensive answer to Corb.  When I tried to re-post it as an edit, the screen said I wasn't allowed, and the post was gone.  I'll be happy as a clam if the post goes up.  I'm a booster here.

The post will speak for itself.  I think I was pretty nice.  If it is gone into the forever limbo, I will reconstruct it painstakingly from memory and re-post it, but my bet is someone can find it or otherwise recover it and put it up where it belongs.



#10 corb

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Posted 30 August 2015 - 05:08 AM

The above answer left out my comprehensive answer to Corb.  When I tried to re-post it as an edit, the screen said I wasn't allowed, and the post was gone.  I'll be happy as a clam if the post goes up.  I'm a booster here.

The post will speak for itself.  I think I was pretty nice.  If it is gone into the forever limbo, I will reconstruct it painstakingly from memory and re-post it, but my bet is someone can find it or otherwise recover it and put it up where it belongs.

 

It's always best to write big paragraphs in the notepad or another word processor first and then to copy them over because the forum is glitchy sometimes. I've lost big posts like that as well and then had to rewrite the whole thing from scratch. I'm not sure it's possible to restore a forum post.

Did it fail to post properly the first time?

Or did you post it and then tried to edit and that's when it went away?
If it didn't post properly the first time it's probably gone. If it was posted and then you somehow deleted it later there's a small chance it could be preserved though I don't think the typical forum software actually does that.

 

I would've given you the link listing the forum moderators but for some reason that doesn't work right now.

 

 

I think I was pretty nice.

And now I'm scared. Nice as opposed to what? :-D



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#11 Anthropositor

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Posted 30 August 2015 - 09:05 AM

Hi Corb, Thanks for reaching out.  Nice means I made eight points, working on not being cruel.  But nicer is just to let it slide, even though this message does not seem to want to post.  I probably tried to answer from my Email.  Probably wont work.  Peace be upon you and yours.







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